Ginkgo modulates noise induced hippocampal damage in male albino rats: a light and electron microscopic study

Noise has been a major problem to mankind and induces many auditory and extra-auditory hazards. This study was carried out to determine the injurious effects of noise on the hippocampus and to show whether Ginkgo biloba has any modulatory effect on hippocampal injury. Twenty-five adult male albino rats were divided into five groups: a control group; a noise group exposed to 100 dB of sound pressure level white noise 4h/day for 4 weeks; a protected group exposed to the same noise level with the administration of a G. biloba extract [50mg/kg daily] for 4 weeks; a recovery group, which was allowed to recover for 4 weeks after noise cessation; and a treated group, administered the same dose of G. biloba for 4 weeks after noise cessation. In the noise-exposed group, the pyramidal cell layer of CA1 and CA3 and the granular cell layer of the dentate gyrus [DG] showed a decrease in thickness compared with the control group, which showed loss and degeneration of many cells, and evidence of increased apoptosis. The protected and treated groups showed improvement in many parameters compared with the recovery group, that is, an increase in the thickness of CA1, CA3, and DG; increase in the surface area of cells; increased vascularity; and a statistically significant decrease in apoptosis compared with the recovery group. Noise exerted detrimental effects on cells of CA1, CA3, and DG of the hippocampus. Although partial spontaneous recovery may occur after cessation of noise exposure, the administration of G. biloba led to a marked decrease in the injurious effect of noise on the hippocampus. This might suggest the probable usefulness of G. biloba in reducing the central hazardous effects in individuals exposed to noise

possible protective role of selenium supplementation on the structure of trhe heart in an experimental model of chronic renal failure: a light and electron microscopic study

Chronic kidney disease [CKD] is a worldwide health hazard with significant morbidity and mortality especially due to cardiovascular complications. This study was conducted to investigate the histological effects of CKD on the structure of the heart and to show the possible protective role of selenium [Se] supplements. Twenty adult male Wistar albino rats were used in this study. They were divided into three groups: group I [the control group] was divided into two subgroups: IA [sham operated], which was subjected to sham operation, and IB [the negative control group], which was left untreated; group II [the nephrectomy group] was subjected to a five-sixth nephrectomy operation to induce renal failure; group III [the Se-treated group] was subjected to a five/sixth nephrectomy operation following which the rats were supplemented with sodium selenite at a dose of 0.04 mg/kg for 10 weeks. At the end of the experiment body weight [BW] and serum creatinine were measured. Heart specimens were processed for light and electron microscopic examination, and morphometric analysis was performed for area percentage of intercellular spaces and collagen fibers. Group II showed significant widening of the interfiber spaces with aggregation of adipocytes, extravasated RBCs, and lymphocytes. There was also significant increase in the area percentage of collagen fibers. Cardiac myocytes appeared swollen, pale, and degenerated, and electron microscopic findings pointed to endothelial dysfunction. Se administration led to significant improvement in BW, creatinine level, and cardiac fibrosis; yet, the heart showed focal pale vacuolated myocytes, wide interfiber spaces, and extravasated blood. CKD led to definite focal degeneration in the cardiac muscle fibers. Se with the dose given improved BW, creatinine level, and cardiac fibrosis but could not offer complete protection against cardiovascular complication

histological study on the effect of pentoxifylline on acute lung injury induced by renal ischemia reperfusion

Kidney ischemia-reperfusion injury [IRI] occurs under many clinical conditions. It leads to acute kidney injury, which may affect various remote but important organs such as the lung. The aim of the present study was to investigate the effect of renal IRI on the lung structure and evaluate the possible protective effect of pentoxifylline [PTX]. Fifteen adult male Wistar rats aged 8-10 weeks and weighing 150-200 g were used in this study. They were divided into the following groups: group I [the control group] was subjected to sham operation; group II [the IRI group] was subjected to renal ischemia by bilateral clamping of the renal pedicles for 45 min and then allowed 24 h of reperfusion. Group III [the PTX-treated group] was given two doses of PTX [40 mg/kg] intraperitoneally and subjected to an ischemia-reperfusion procedure as performed in group II. Lung specimens were processed for light and electron microscopic examination. The mean thickness of the interalveolar septa and the mean number of type-II pneumocytes were measured. Group II showed diffuse lung injury affecting mainly the alveoli, which appeared flooded with exudate and red blood cells, which also extravasated in the interstitium. There was vacuolation of the cytoplasm of both type-I and type-II pneumocytes with significant increase in the number of type-II cells and depletion of lamellar bodies. Significant increase in the mean thickness of the interalveolar septa was detected and it showed infiltration by macrophages and neutrophils. PTX caused marked improvement in the lung structure after ischemia-reperfusion. Most of the alveoli appeared empty and a few of them showed minimal red blood cells and macrophages. Thin interalveolar septa were detected with thickness comparable to that of the control group. Renal IRI caused alteration in the lung structure, which was ameliorated by PTX administration

possible therapeutic effect of 'chaetomium globosum' fungal extract on experimentally induced rheumatoid arthritis

Rheumatoid arthritis [RA] is an autoimmune disease that leads to chronic inflammation in the joints with subsequent cartilage and bone destruction. RA induces a massive burden on health services worldwide. This study was designed to evaluate the possible therapeutic effect of 'Chaetomium globosum' extract in the treatment of RA in a rat model. Forty male Wistar albino rats aged 8-10 weeks were divided into four groups of 10 rats each. The control group [group I] was injected subcutaneously with 0.1 ml of saline. RA was induced in the other three groups [groups II, III, and IV] by single subcutaneous injection of 0.1 ml of complete Freund's adjuvant in the footpad of the right hind paw. Group II was induced with arthritis and left untreated. Rats in groups III and IV were treated by administering either C. globosum 10 micro g/kg or methotrexate [MTX] 0.3 mg/kg subcutaneously twice weekly for 2 weeks from day 12 after induction of arthritis. Animals of all groups were sacrificed on day 28 from the start of the experiment. The ankle joints were processed and stained with H and E, Masson's trichrome, and immunohistochemical stain for inducible nitric oxide synthase. Specimens were also processed for transmission electron microscopic study. Untreated arthritic rats revealed paw swelling, synovial hyperplasia, inflammatory infiltration, collagen accumulation, cartilage degradation, bone destruction, and significant increase in inducible nitric oxide synthase-positive chondrocytes. Transmission electron microscopic examination confirmed these results. The present study demonstrated for the first time that C. globosum significantly reduced all the clinical and histopathological changes of arthritis similar to MTX. C. globosum extract had therapeutic effects similar to the well-established drug MTX and could be devoid of its serious side effects.

Evaluation of honey protective effect on lead induced oxidative stress in rats

Lead toxicity is a worldwide health problem due to continuous exposure of the population to lead in the environment especially workers in industries. It affects many body organs especially the liver and kidneys. The aim of this study is to investigate the protective effect of natural honey against lead induced oxidative stress, hepatotoxicity and nephrotoxicity. Forty male albino rats were used in this study divided into 4 equal groups. Group [I] the control group were given distilled water orally for 4 weeks. Group [II] rats were given 1.5 ml/kg natural honey orally for 4 weeks. Group [III] rats were given lead acetate [0.2%] in drinking water for 4 weeks .Group [IV] rats were given lead acetate [0.2%] in drinking water and 1.5 ml/kg natural honey orally for 4 weeks. Blood and tissue samples were taken after four weeks. Lipid peroxidation product, malondialdehyde [MDA] in plasma, liver and kidney were determined, blood glutathione peroxidase activity [GPx] and serum nitric oxide [NO] levels were also measured, Liver function tests [serum alkaline phosphatase [ALP], aspartate transaminase [AST] and alanine transaminase[ALT] were measured. Kidney function tests [blood urea and s. creatinine] were estimated. Histopathological examination of liver and kidney sections was performed. showed significant [P>0.01] increase in the mean MDA of plasma. liver and kidney of lead acetate group [Group III] with decreased antioxidant enzyme activity [GPx] activity and [NO] and increase levels of AST, ALT, ALP, urea and serum creatinine together with histopathological changes in liver and kidney sections. Honey alleviated the increased MDA levels, and ameliorate the elevated AST, ALT, ALP, urea and serum creatinine in the combination group. The present study revealed that natural honey could diminish the adverse effects of lead acetate as shown in the histological analysis of rat livers and kidneys. The present results indicated that natural honey can modulate the damage in liver and kidney cells from oxidative stress induced by lead toxicity in tart